Anti-Decoy Receptor 3 (DcR3) [Clone MD3B1] – HRPO

Full length human DcR3

This HRP-conjugated antibody is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4, 1% BSA. (Warning: Use of sodium azide as a preservative will inhibit the enzyme activity of horseradish peroxidase)

Liquid

This horseradish peroxidase conjugated monoclonal antibody is stable when stored at 2-8°C. Do not freeze.

Research Use Only

2 – 8° C Wet Ice

MD3B1 activity is directed against DcR3.

DcR3 (also known as TR6, M68, and TNFRSF6B) is a member of the tumor necrosis factor receptor superfamily^1,2. DcR3 acts as a soluble decoy receptor that can modulate the effect of TNF surface receptors by competing for binding to the TNF family ligands Fas ligand, LIGHT, and TL1A. DcR3 also plays a role in the immune system by modulating T cell responses as well as differentiation and maturation of dendritic cells. Additionally, DcR3 likely plays a role in keratinocyte differentiation and egg fertilization².

DcR3 is normally expressed at very low levels but is upregulated in tumors and inflammatory tissues². Accordingly, DcR3 is regarded as a potential biomarker for cancer metastasis and as a predictor of inflammatory disease progression. In tumors, upregulation of DcR3 prevents apoptosis and promotes growth, invasion, and angiogenesis. Additionally, upregulation of DcR3 as part of the TL1A/death receptor 3 (DR3/TNFRSF25) axis is important to the pathogenesis of various inflammatory and autoimmune diseases including silicosis, bacterial infection, coronary artery disease, inflammatory bowel disease, osteoarthritis, and rheumatoid arthritis. DcR3 can also be upregulated by ultraviolet light, epidermal growth factor, and transforming growth factor (TGF)-α.

DcR3 is expressed in a wide variety of normal human tissues as well as various cancers. DcR3 is detectable in granulosa cells, endometrial cells, theca cells, undifferentiated primary keratinocytes, monocytes, dendritic cells, synovial fluids, and chondrocytes, among others.

FasL, LIGHT, and TL1A

1 Chen J, Zhang L, Kim S. J Immunol Methods. 285(1):63-70. 2004.
2 Hsieh SL, Lin WW. J Biomed Sci. 24(1):39. 2017.